Burn-Induced Acute Kidney Injury-Two-Lane Road: From Molecular to Clinical Aspects

Abstract

Severe burn injuries lead to acute kidney injury (AKI) development, increasing the mortality risk up to 28-100%. In addition, there is an increase in hospitalization days and complications appearance. Various factors are responsible for acute or late AKI debut, like hypovolemia, important inflammatory response, excessive load of denatured proteins, sepsis, and severe organic dysfunction. The main measure to improve the prognosis of these patients is rapidly recognizing this condition and reversing the underlying events. For this reason, different renal biomarkers have been studied over the years for early identification of burn-induced AKI, like neutrophil gelatinase-associated lipocalin (NGAL), cystatin C, kidney injury molecule-1 (KIM-1), tissue inhibitor of metalloproteinase-2 (TIMP-2), interleukin-18 (IL-18), and insulin-like growth factor-binding protein 7 (IGFBP7). The fundamental purpose of these studies is to find a way to recognize and prevent acute renal injury progression early in order to decrease the risk of mortality and chronic kidney disease (CKD) onset.

Keywords: IGFBP7; KIM-1; NGAL; TIMP-2; acute kidney injury; burn; cystatin C.

Figure 1

Etiology of burn-induced acute kidney injury. Notes: AKI—acute kidney injury; MODS—multiple organ dysfunction syndrome.

Figure 2

Main risk factors of burned-induced AKI. Notes: ABSI—the abbreviated burn severity index; APACHE II—acute physiology and chronic health evaluation II; SOFA—sequential organ failure assessment; TBSA—total body surface area.

Figure 3

The main feature of usual biomarkers used in burn-induced AKI diagnosis. Notes: Levels are measured in urine. NGAL—neutrophil gelatinase-associated lipocalin; KIM-1—kidney injury molecule-1; TIMP-2—tissue inhibitor of metalloproteinase-2; IGFBP7—insulin-like growth factor-binding protein; IL-18—interleukin-18; PCT—proximal convoluted tubule, CD—collecting duct.

Figure 4

The role of novel biomarkers in identifying the site of AKI insult. Notes: IGFBP7 = insulin-like growth factor-binding protein 7; IL-18 = interleukin-18; KIM-1 = kidney injury molecule-1; L-FABP = liver-type fatty acid-binding protein; NGAL = neutrophil gelatinase-associated lipocalin; SCr = serum creatinine; SCyst-C = serum cystatin-C; TIMP2 = tissue inhibitor of metalloproteinase-2; UAlb = urine albumin; UCyst-C = urine cystatin-C (Modified after [69,101]).